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===Histology===
===Histology===
Autoimmune hepatitis can be characterized histologically by the following nonspecific findings:<ref>{{Cite journal|last=Hofer|first=H.|last2=Oesterreicher|first2=C.|last3=Wrba|first3=F.|last4=Ferenci|first4=P.|last5=Penner|first5=E.|date=2006-03|title=Centrilobular necrosis in autoimmune hepatitis: a histological feature associated with acute clinical presentation|url=https://pubmed.ncbi.nlm.nih.gov/16505273|journal=Journal of Clinical Pathology|volume=59|issue=3|pages=246–249|doi=10.1136/jcp.2005.029348|issn=0021-9746|pmc=1860344|pmid=16505273}}</ref><ref>{{Cite journal|last=Verdonk|first=Robert C.|last2=Lozano|first2=Mallaki F.|last3=van den Berg|first3=Aad P.|last4=Gouw|first4=Annette S. H.|date=2016-09|title=Bile ductal injury and ductular reaction are frequent phenomena with different significance in autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/26849025|journal=Liver International: Official Journal of the International Association for the Study of the Liver|volume=36|issue=9|pages=1362–1369|doi=10.1111/liv.13083|issn=1478-3231|pmid=26849025}}</ref><ref>{{Cite journal|last=Abe|first=Masanori|last2=Onji|first2=Morikazu|last3=Kawai-Ninomiya|first3=Keiko|last4=Michitaka|first4=Kojiro|last5=Matsuura|first5=Bunzo|last6=Hiasa|first6=Yoichi|last7=Horiike|first7=Norio|date=2007-02|title=Clinicopathologic features of the severe form of acute type 1 autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/17218164|journal=Clinical Gastroenterology and Hepatology: The Official Clinical Practice Journal of the American Gastroenterological Association|volume=5|issue=2|pages=255–258|doi=10.1016/j.cgh.2006.10.011|issn=1542-7714|pmid=17218164}}</ref><ref>{{Cite journal|last=Stravitz|first=R. Todd|last2=Lefkowitch|first2=Jay H.|last3=Fontana|first3=Robert J.|last4=Gershwin|first4=M. Eric|last5=Leung|first5=Patrick S. C.|last6=Sterling|first6=Richard K.|last7=Manns|first7=Michael P.|last8=Norman|first8=Gary L.|last9=Lee|first9=William M.|last10=Acute Liver Failure Study Group|date=2011-02|title=Autoimmune acute liver failure: proposed clinical and histological criteria|url=https://pubmed.ncbi.nlm.nih.gov/21274872|journal=Hepatology (Baltimore, Md.)|volume=53|issue=2|pages=517–526|doi=10.1002/hep.24080|issn=1527-3350|pmc=3080034|pmid=21274872}}</ref>
Histological features supportive of a diagnosis of autoimmune hepatitis include:<ref>{{cite journal |last1=Webb |first1=GJ |last2=Hirschfield |first2=GM |last3=Krawitt |first3=EL |last4=Gershwin |first4=ME |title=Cellular and Molecular Mechanisms of Autoimmune Hepatitis. |journal=Annual Review of Pathology |date=24 January 2018 |volume=13 |pages=247–292 |doi=10.1146/annurev-pathol-020117-043534 |pmid=29140756}}</ref>


* A mixed inflammatory infiltrate centered on the portal tract
* Portal mononuclear cell infiltrate that invades the boundary surrounding the portal triad and infiltrates the surrounding lobule.
* Periportal lesions, also known as interface hepatitis, that spare the biliary tree (may include centrizonal necrosis).
** The inflammatory infiltrate may breach the interface between the portal tract and liver parenchyma: so-called interface hepatitis
* Bile duct abnormalities (cholangitis, ductal injury, ductular reaction) can be seen and should prompt evaluation for primary biliary cholangitis or sarcoidosis if granulomas are observed.
** The most numerous cell in the infiltrate is the [[T helper cell|CD4-positive T cell]].
* Plasma cell infiltrate, rosettes of hepatocytes, and multinucleated giant cells.
** [[Plasma cell]]s may be present within the infiltrate. These are predominantly IgG-secreting.
* Varying degrees of fibrosis (except in the mildest form of autoimmune hepatitis). Bridging fibrosis that connects the portal and central areas can distort the structure of the hepatic lobule and result in cirrhosis.
** [[Eosinophil]]s may be present within the infiltrate.
** Emperipolesis, where there is penetration of one cell through another, within the inflammatory infiltrate
* Varying degrees of [[necrosis]] of periportal [[hepatocyte]]s.
** In more severe cases, necrosis may become confluent with necrotic bridges forming between central veins.
* Hepatocyte [[apoptosis]] manifest as acidophils or apoptotic bodies.
* Rosettes of regenerating hepatocytes.
* Any degree of [[fibrosis]] from none to advanced [[cirrhosis]]
* Biliary inflammation without destruction of biliary epithelial cells in a minority of cases.


===Diagnostic scoring===
===Diagnostic scoring===
The Internal Autoimmune Hepatitis Group developed a standardized scoring system for clinical diagnosis in population studies but lacks value in individualized cases.<ref>{{Cite journal|last=Alvarez|first=F.|last2=Berg|first2=P. A.|last3=Bianchi|first3=F. B.|last4=Bianchi|first4=L.|last5=Burroughs|first5=A. K.|last6=Cancado|first6=E. L.|last7=Chapman|first7=R. W.|last8=Cooksley|first8=W. G.|last9=Czaja|first9=A. J.|last10=Desmet|first10=V. J.|last11=Donaldson|first11=P. T.|date=1999-11|title=International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/10580593|journal=Journal of Hepatology|volume=31|issue=5|pages=929–938|doi=10.1016/s0168-8278(99)80297-9|issn=0168-8278|pmid=10580593}}</ref> A simplified scoring system for clinical use incorporates titers of autoantibodies, total IgG levels, liver histology, and the exclusion of viral hepatitis for diagnostic scoring.<ref>{{Cite journal|last=Hennes|first=Elke M.|last2=Zeniya|first2=Mikio|last3=Czaja|first3=Albert J.|last4=Parés|first4=Albert|last5=Dalekos|first5=George N.|last6=Krawitt|first6=Edward L.|last7=Bittencourt|first7=Paulo L.|last8=Porta|first8=Gilda|last9=Boberg|first9=Kirsten M.|last10=Hofer|first10=Harald|last11=Bianchi|first11=Francesco B.|date=2008-07|title=Simplified criteria for the diagnosis of autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/18537184|journal=Hepatology (Baltimore, Md.)|volume=48|issue=1|pages=169–176|doi=10.1002/hep.22322|issn=1527-3350|pmid=18537184}}</ref>
Expert opinion has been summarized by the International Autoimmune Hepatitis Group, which has published criteria which utilize clinical, laboratory, and histological data that can be used to help determine if a patient has autoimmune hepatitis.<ref name="pmid10580593">{{cite journal |vauthors=Alvarez F, Berg PA, Bianchi FB |title=International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis |journal=[[J. Hepatol.]] |volume=31 |issue=5 |pages=929–38 |date=November 1999 |pmid=10580593 |doi= 10.1016/S0168-8278(99)80297-9|display-authors=etal}}</ref>
A calculator based on those criteria is available online.<ref name="urlAutoimmune Hepatitis Calculator">{{cite web |url=http://www.napervillegi.com/contrivances/aihcalc.html |title=Autoimmune Hepatitis Calculator |access-date=2008-05-09}}</ref>

===Overlap===
Overlapping presentation with [[primary biliary cholangitis]] and [[primary sclerosing cholangitis]] has been observed.<ref name="pmid17486048">{{cite journal |author=Washington MK |title=Autoimmune liver disease: overlap and outliers |journal=[[Mod. Pathol.]] |volume=20 Suppl 1 |pages=S15–30 |date=February 2007 |pmid=17486048 |doi=10.1038/modpathol.3800684|doi-access=free }}</ref>


===Classification===
===Classification===
Four subtypes of autoimmune hepatitis are recognised, but the clinical utility of distinguishing subtypes is limited.
On the basis of detected autoantibodies, autoimmune hepatitis can be classified into three subtypes but have no distinct clinical presentations.


* Type 1 autoimmune hepatitis. Positive antibodies include:<ref>{{Cite journal|last=Czaja|first=A. J.|last2=Morshed|first2=S. A.|last3=Parveen|first3=S.|last4=Nishioka|first4=M.|date=1997-09|title=Antibodies to single-stranded and double-stranded DNA in antinuclear antibody-positive type 1-autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/9303484|journal=Hepatology (Baltimore, Md.)|volume=26|issue=3|pages=567–572|doi=10.1002/hep.510260306|issn=0270-9139|pmid=9303484}}</ref><ref>{{Cite journal|last=Terjung|first=B.|last2=Spengler|first2=U.|last3=Sauerbruch|first3=T.|last4=Worman|first4=H. J.|date=2000-08|title="Atypical p-ANCA" in IBD and hepatobiliary disorders react with a 50-kilodalton nuclear envelope protein of neutrophils and myeloid cell lines|url=https://pubmed.ncbi.nlm.nih.gov/10930366|journal=Gastroenterology|volume=119|issue=2|pages=310–322|doi=10.1053/gast.2000.9366|issn=0016-5085|pmid=10930366}}</ref>
* Type 1 AIH. Positive ANA and SMA,<ref name="pmid18528935">{{cite journal |vauthors=Bogdanos DP, Invernizzi P, Mackay IR, Vergani D |title=Autoimmune liver serology: Current diagnostic and clinical challenges |journal=World J. Gastroenterol. |volume=14 |issue=21 |pages=3374–3387 |date=June 2008 |pmid=18528935 |doi= 10.3748/wjg.14.3374|url=http://www.wjgnet.com/1007-9327/14/3374.asp |pmc=2716592}}</ref> elevated [[immunoglobulin G]] (classic form, responds well to low dose steroids);
** Antinuclear antibody (ANA)
* Type 2 AIH. Positive [[Liver kidney microsomal type 1 antibody|LKM-1]] (typically female children and teenagers; disease can be severe), [[Anti-LKM antibody|LKM-2]] or [[Anti-LKM antibody|LKM-3]];
** Anti-smooth muscle antibody (ASMA) - 65% of people
* Type 3 AIH. Positive antibodies against [[soluble liver antigen]]<ref name="urlautoimmune hepatitis">{{cite web |url=http://www.meddean.luc.edu/Lumen/MedEd/orfpath/autoimmune%20hepatitis.htm |title=autoimmune hepatitis }}</ref> (this group behaves like group 1)<ref name="urlMedscape & eMedicine Log In">{{cite web |url=http://www.medscape.com/viewarticle/445619_14 |title=Medscape & eMedicine Log In }}</ref> (anti-SLA, anti-LP)
** Anti-actin antibodies
* AIH with no autoantibodies detected (~20%){{Citation needed|date=July 2008}} (of debatable validity/importance)
** Anti-mitochondrial antibodies - rare except for overlap syndromes with [[primary biliary cholangitis]]
** Anti-soluble liver antigen/liver pancreas antibody antigen - 20% of people
** Anti-double stranded DNA - 30% of people
** Atypical perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)
* Type 2 autoimmune hepatitis. Positive antibodies include:<ref>{{Cite journal|last=Bridoux-Henno|first=Laure|last2=Maggiore|first2=Giuseppe|last3=Johanet|first3=Catherine|last4=Fabre|first4=Monique|last5=Vajro|first5=Pietro|last6=Dommergues|first6=Jean-Paul|last7=Reinert|first7=Philippe|last8=Bernard|first8=Olivier|date=2004-09|title=Features and outcome of autoimmune hepatitis type 2 presenting with isolated positivity for anti-liver cytosol antibody|url=https://pubmed.ncbi.nlm.nih.gov/15354284|journal=Clinical Gastroenterology and Hepatology: The Official Clinical Practice Journal of the American Gastroenterological Association|volume=2|issue=9|pages=825–830|doi=10.1016/s1542-3565(04)00354-4|issn=1542-3565|pmid=15354284}}</ref><ref>{{Cite journal|last=Bridoux-Henno|first=Laure|last2=Maggiore|first2=Giuseppe|last3=Johanet|first3=Catherine|last4=Fabre|first4=Monique|last5=Vajro|first5=Pietro|last6=Dommergues|first6=Jean-Paul|last7=Reinert|first7=Philippe|last8=Bernard|first8=Olivier|date=2004-09|title=Features and outcome of autoimmune hepatitis type 2 presenting with isolated positivity for anti-liver cytosol antibody|url=https://pubmed.ncbi.nlm.nih.gov/15354284|journal=Clinical Gastroenterology and Hepatology: The Official Clinical Practice Journal of the American Gastroenterological Association|volume=2|issue=9|pages=825–830|doi=10.1016/s1542-3565(04)00354-4|issn=1542-3565|pmid=15354284}}</ref>
** Liver Kidney Microsomal antibody (LKM-1)
** Anti-liver cytosol antibody-1 (SLC-1)
* Autoantibody negative autoimmune hepatitis.<ref>{{Cite journal|last=Heneghan|first=Michael A.|last2=Yeoman|first2=Andrew D.|last3=Verma|first3=Sumita|last4=Smith|first4=Alastair D.|last5=Longhi|first5=Maria Serena|date=2013-10-26|title=Autoimmune hepatitis|url=https://pubmed.ncbi.nlm.nih.gov/23768844|journal=Lancet (London, England)|volume=382|issue=9902|pages=1433–1444|doi=10.1016/S0140-6736(12)62163-1|issn=1474-547X|pmid=23768844}}</ref>
** Lack positive ANA, ASMA, LKM-1, etc. antibody panels but present with clinical features of autoimmune hepatitis that resolve with standard treatment.


==Treatment==
==Treatment==

Revision as of 02:25, 21 January 2022

Autoimmune hepatitis
Micrograph showing a lymphoplasmacytic interface hepatitis—the characteristic histomorphologic finding of autoimmune hepatitis. Liver biopsy. H&E stain.
SpecialtyGastroenterology, hepatology Edit this on Wikidata
SymptomsOften asymptomatic, fatigue, right upper abdominal pain, anorexia, nausea, jaundice, joint pain, rash
Usual onset40-50 years of age
TypesType 1, type 2, type 3, seronegative
Risk factorsFemale gender, additional autoimmune disease
Diagnostic methodLiver biopsy
Differential diagnosisPrimary biliary cholangitis
Primary sclerosing cholangitis
TreatmentPrednisone, Azathioprine
FrequencyIncidence 1-2 per 100,000 per year
Prevalence 10-20 per 100,000

Autoimmune hepatitis, formerly known as lupoid hepatitis, plasma cell hepatitis, or autoimmune chronic active hepatitis, is a chronic, autoimmune disease of the liver that occurs when the body's immune system attacks liver cells, causing the liver to be inflamed. Common initial symptoms may include fatigue, nausea, muscle aches, or weight loss or signs of acute liver inflammation including fever, jaundice, and right upper quadrant abdominal pain. Individuals with autoimmune hepatitis often have no initial symptoms and the disease may be detected by abnormal liver function tests and increased protein levels during routine bloodwork or the observation of an abnormal-looking liver during abdominal surgery.[1]

Anomalous presentation of MHC class II receptors on the surface of liver cells,[2] possibly due to genetic predisposition or acute liver infection, causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis. This abnormal immune response results in inflammation of the liver, which can lead to further symptoms and complications such as fatigue and cirrhosis.[3] The disease is most often diagnosed in patients in their late teens or early 20s and between the ages of 40 and 50. It affects women more commonly than men.[4]

Signs and symptoms

Autoimmune hepatitis may present completely asymptomatic (12–35% of the cases), with signs of chronic liver disease, or acute or even fulminant hepatic failure.[5][6]

People usually present with one or more nonspecific, long-lasting symptoms such as fatigue, general ill health, lethargy, weight loss, mild right upper quadrant abdominal pain, malaise, anorexia, itching, nausea, jaundice or joint pain especially affecting the small joints. Rarely, rash or unexplained fever may appear. In women, the absence of menstruation (amenorrhoea) is a frequent feature. Physical examination may be normal, but it may also reveal signs and symptoms of chronic liver disease. Many people have only laboratory abnormalities as their initial presentation, as unexplained increase in transaminases and are diagnosed during an evaluation for other reasons. Others have already developed cirrhosis at diagnosis.[6] Of note, alkaline phosphatase and bilirubin are usually normal.

Autoimmune hepatitis may overlap with other autoimmune conditions, mainly type 1 diabetes mellitus, ulcerative colitis, lupus, celiac disease, vasculitis, and autoimmune thyroiditis.[5]

Cause

60% of patients have chronic hepatitis that may mimic viral hepatitis, but without serologic evidence of a viral infection. The disease is strongly associated with anti-smooth muscle autoantibodies. The current theory for the cause is that the disease is triggered by an environmental cause (virus, drugs, herbs, immunizations) in a genetically predisposed individual. The exact genes and triggers responsible remain undefined, but studies show association of early-onset, severe disease with the HLA-DR3 serotype and late-onset disease with the HLA-DR4 serotype.[7]

Diagnosis

The diagnosis of autoimmune hepatitis is best achieved with a combination of clinical, laboratory, and histological findings after excluding other etiological factors (e.g. viral [such as the Epstein-Barr virus], hereditary, metabolic, cholestatic, and drug-induced liver diseases). The requirement for histological examination necessitates a liver biopsy, typically performed with a needle by the percutaneous route, to provide liver tissue.

Autoantibodies

A number of specific antibodies found in the blood (antinuclear antibody (ANA), anti-smooth muscle antibody (SMA), anti-liver kidney microsomal antibodies (LKM-1, LKM-2, LKM-3), anti soluble liver antigen (SLA), liver–pancreas antigen (LP), and anti-mitochondrial antibody (AMA)) are of use, as is finding an increased immunoglobulin G level. The presence of anti-mitochondrial antibody is more suggestive of primary biliary cholangitis. Hypergammaglobulinemia is also of diagnostic value.[8]

Histology

Autoimmune hepatitis can be characterized histologically by the following nonspecific findings:[9][10][11][12]

  • Portal mononuclear cell infiltrate that invades the boundary surrounding the portal triad and infiltrates the surrounding lobule.
  • Periportal lesions, also known as interface hepatitis, that spare the biliary tree (may include centrizonal necrosis).
  • Bile duct abnormalities (cholangitis, ductal injury, ductular reaction) can be seen and should prompt evaluation for primary biliary cholangitis or sarcoidosis if granulomas are observed.
  • Plasma cell infiltrate, rosettes of hepatocytes, and multinucleated giant cells.
  • Varying degrees of fibrosis (except in the mildest form of autoimmune hepatitis). Bridging fibrosis that connects the portal and central areas can distort the structure of the hepatic lobule and result in cirrhosis.

Diagnostic scoring

The Internal Autoimmune Hepatitis Group developed a standardized scoring system for clinical diagnosis in population studies but lacks value in individualized cases.[13] A simplified scoring system for clinical use incorporates titers of autoantibodies, total IgG levels, liver histology, and the exclusion of viral hepatitis for diagnostic scoring.[14]

Classification

On the basis of detected autoantibodies, autoimmune hepatitis can be classified into three subtypes but have no distinct clinical presentations.

  • Type 1 autoimmune hepatitis. Positive antibodies include:[15][16]
    • Antinuclear antibody (ANA)
    • Anti-smooth muscle antibody (ASMA) - 65% of people
    • Anti-actin antibodies
    • Anti-mitochondrial antibodies - rare except for overlap syndromes with primary biliary cholangitis
    • Anti-soluble liver antigen/liver pancreas antibody antigen - 20% of people
    • Anti-double stranded DNA - 30% of people
    • Atypical perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)
  • Type 2 autoimmune hepatitis. Positive antibodies include:[17][18]
    • Liver Kidney Microsomal antibody (LKM-1)
    • Anti-liver cytosol antibody-1 (SLC-1)
  • Autoantibody negative autoimmune hepatitis.[19]
    • Lack positive ANA, ASMA, LKM-1, etc. antibody panels but present with clinical features of autoimmune hepatitis that resolve with standard treatment.

Treatment

The choice for medical treatment should be based on the individual's severity of symptoms, quantitative elevation of liver enzymes and antibody levels, findings on liver biopsy, and ability to tolerate side effects of medical therapy.

Generally, treatment is not required in asymptomatic patients with normal liver enzyme and antibody levels and liver biopsies that do not demonstrate inflammation because these patients are at a low risk of disease progression. In symptomatic individuals with evidence of interface hepatitis and necrosis on liver biopsy, it is recommended to offer treatment especially if the patient is young and can tolerate the side effects of medical therapy.

The mainstay of treatment involves the use of immunosuppressive glucocorticoids such as prednisone during acute episodes and resolution of symptoms can be achieved in up to 60–80% of cases, although many will eventually experience a relapse.[20] In individuals with moderate to severe disease who may not tolerate glucocorticoids, lower dose prednisone monotherapy or combination with azathioprine is a reasonable alternative. Budesonide has been shown to be more effective in inducing remission than prednisone, but evidence is scare and more data is needed before it can be routinely recommended.[21] Those with autoimmune hepatitis who do not respond to glucocorticoids and azathioprine may be given other immunosuppressives like mycophenolate, ciclosporin, tacrolimus, methotrexate, etc. Liver transplantation may be required if patients do not respond to drug therapy or when patients present with fulminant liver failure.[22]

Prognosis

Without treatment, the 10-year survival rate for individuals with symptomatic autoimmune hepatitis is 50%. However, with treatment, the 10-year survival rate is above 90%. Despite the benefits of treatment, people with autoimmune hepatitis generally have a lower transplant-free survival than the general population.[23][24][25]

Additionally, presentation and response to therapy appears to differ according to race. For instance, African Americans appear to present with a more aggressive disease that is associated with worse outcomes.[26][27] If untreated, the mortality rate for severe autoimmune hepatitis may be as high as 40 percent.[4]

Outcomes with liver transplant are generally favorable, with a five-year survival greater than 80 percent.[4] There has been strong evidence that patients with autoimmune hepatitis can develop mental health disorders like Schizophrenia and Bipolar disorder later in their life.[28]

Epidemiology

Autoimmune hepatitis has an incidence of 1-2 per 100,000 per year, and a prevalence of 10-20/100,000. As with most other autoimmune diseases, it affects women much more often than men (70%).[29]

The disease may occur in any ethnic group and at any age, but is most often diagnosed in patients between age 40 and 50.[4]

History

Autoimmune hepatitis was previously called "lupoid" hepatitis. It was originally described in the early 1950s.[30]

Most patients do have an associated autoimmune disorder such as systemic lupus erythematosus. Thus, its name was previously lupoid hepatitis.

Because the disease has multiple different forms, and is not always associated with systemic lupus erythematosus, lupoid hepatitis is no longer used. The current name at present is autoimmune hepatitis (AIH).

References

  1. ^ Czaja, AJ (May 2004). "Autoimmune liver disease". Current Opinion in Gastroenterology. 20 (3): 231–40. doi:10.1097/00001574-200405000-00007. PMID 15703647.
  2. ^ Franco, A; Barnaba, V; Natali, P; Balsano, C; Musca, A; Balsano, F (May–June 1988). "Expression of class I and class II major histocompatibility complex antigens on human hepatocytes". Hepatology. 8 (3): 449–54. doi:10.1002/hep.1840080302. PMID 2453428. S2CID 23341082.
  3. ^ National Digestive Diseases Information Clearinghouse. "Digestive Disease: Autoimmune Hepatitis". Archived from the original on 15 September 2010. Retrieved October 9, 2010.
  4. ^ a b c d Manns, MP; Czaja, AJ; Gorham, JD; Krawitt, EL; Mieli-Vergani, G; Vergani, D; Vierling, JM; American Association for the Study of Liver, Diseases (June 2010). "Diagnosis and management of autoimmune hepatitis". Hepatology. 51 (6): 2193–213. doi:10.1002/hep.23584. PMID 20513004. S2CID 30356212.
  5. ^ a b Than NN, Jeffery HC, Oo YH (2016). "Autoimmune Hepatitis: Progress from Global Immunosuppression to Personalised Regulatory T Cell Therapy". Can J Gastroenterol Hepatol (Review). 2016: 1–12. doi:10.1155/2016/7181685. PMC 4904688. PMID 27446862.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ^ a b Zachou K, Muratori P, Koukoulis GK, Granito A, Gatselis N, Fabbri A, et al. (2013). "Review article: autoimmune hepatitis -- current management and challenges". Aliment Pharmacol Ther (Review). 38 (8): 887–913. doi:10.1111/apt.12470. PMID 24010812. S2CID 29295458.Open access icon
  7. ^ "Autoimmune hepatitis | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program". rarediseases.info.nih.gov. Retrieved 2018-04-17.
  8. ^ Alvarez, F; Berg, PA; Bianchi, FB; Bianchi, L; Burroughs, AK; Cancado, EL; Chapman, RW; Cooksley, WG; Czaja, AJ; Desmet, VJ; Donaldson, PT; Eddleston, AL; Fainboim, L; Heathcote, J; Homberg, JC; Hoofnagle, JH; Kakumu, S; Krawitt, EL; Mackay, IR; MacSween, RN; Maddrey, WC; Manns, MP; McFarlane, IG; Meyer zum Büschenfelde, KH; Zeniya, M (November 1999). "International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis". Journal of Hepatology. 31 (5): 929–38. doi:10.1016/S0168-8278(99)80297-9. PMID 10580593.
  9. ^ Hofer, H.; Oesterreicher, C.; Wrba, F.; Ferenci, P.; Penner, E. (2006-03). "Centrilobular necrosis in autoimmune hepatitis: a histological feature associated with acute clinical presentation". Journal of Clinical Pathology. 59 (3): 246–249. doi:10.1136/jcp.2005.029348. ISSN 0021-9746. PMC 1860344. PMID 16505273. {{cite journal}}: Check date values in: |date= (help)
  10. ^ Verdonk, Robert C.; Lozano, Mallaki F.; van den Berg, Aad P.; Gouw, Annette S. H. (2016-09). "Bile ductal injury and ductular reaction are frequent phenomena with different significance in autoimmune hepatitis". Liver International: Official Journal of the International Association for the Study of the Liver. 36 (9): 1362–1369. doi:10.1111/liv.13083. ISSN 1478-3231. PMID 26849025. {{cite journal}}: Check date values in: |date= (help)
  11. ^ Abe, Masanori; Onji, Morikazu; Kawai-Ninomiya, Keiko; Michitaka, Kojiro; Matsuura, Bunzo; Hiasa, Yoichi; Horiike, Norio (2007-02). "Clinicopathologic features of the severe form of acute type 1 autoimmune hepatitis". Clinical Gastroenterology and Hepatology: The Official Clinical Practice Journal of the American Gastroenterological Association. 5 (2): 255–258. doi:10.1016/j.cgh.2006.10.011. ISSN 1542-7714. PMID 17218164. {{cite journal}}: Check date values in: |date= (help)
  12. ^ Stravitz, R. Todd; Lefkowitch, Jay H.; Fontana, Robert J.; Gershwin, M. Eric; Leung, Patrick S. C.; Sterling, Richard K.; Manns, Michael P.; Norman, Gary L.; Lee, William M.; Acute Liver Failure Study Group (2011-02). "Autoimmune acute liver failure: proposed clinical and histological criteria". Hepatology (Baltimore, Md.). 53 (2): 517–526. doi:10.1002/hep.24080. ISSN 1527-3350. PMC 3080034. PMID 21274872. {{cite journal}}: Check date values in: |date= (help)
  13. ^ Alvarez, F.; Berg, P. A.; Bianchi, F. B.; Bianchi, L.; Burroughs, A. K.; Cancado, E. L.; Chapman, R. W.; Cooksley, W. G.; Czaja, A. J.; Desmet, V. J.; Donaldson, P. T. (1999-11). "International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis". Journal of Hepatology. 31 (5): 929–938. doi:10.1016/s0168-8278(99)80297-9. ISSN 0168-8278. PMID 10580593. {{cite journal}}: Check date values in: |date= (help)
  14. ^ Hennes, Elke M.; Zeniya, Mikio; Czaja, Albert J.; Parés, Albert; Dalekos, George N.; Krawitt, Edward L.; Bittencourt, Paulo L.; Porta, Gilda; Boberg, Kirsten M.; Hofer, Harald; Bianchi, Francesco B. (2008-07). "Simplified criteria for the diagnosis of autoimmune hepatitis". Hepatology (Baltimore, Md.). 48 (1): 169–176. doi:10.1002/hep.22322. ISSN 1527-3350. PMID 18537184. {{cite journal}}: Check date values in: |date= (help)
  15. ^ Czaja, A. J.; Morshed, S. A.; Parveen, S.; Nishioka, M. (1997-09). "Antibodies to single-stranded and double-stranded DNA in antinuclear antibody-positive type 1-autoimmune hepatitis". Hepatology (Baltimore, Md.). 26 (3): 567–572. doi:10.1002/hep.510260306. ISSN 0270-9139. PMID 9303484. {{cite journal}}: Check date values in: |date= (help)
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  28. ^ Jeyanthi, Dr Keerthana Mani; Katta, Dr Maanya Rajasree; Mishra, Dr Sakshi; Christopher, Dr Joana; Jain, Dr Aakanksh; Jamil, Dr Maria (2021-06-12). "Evaluation of Autoimmune Diseases with Mental Health Disorders: An Original Research". Annals of the Romanian Society for Cell Biology. 25 (6): 10860–10864.
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